Massage & Bodywork

MARCH | APRIL 2019

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technique
THE SOMATIC EDGE
Understanding Inflammation and Pain
By Til Luchau
Chances are very good that if
your client has pain or discomfort,
inflammation is to blame; if not
wholly, then at least in large part.
Inflammation is directly involved in the
pain conditions ranging from sciatica
to arthritis, whiplash to tennis elbow,
and from migraines to postexercise
muscle soreness. So how exactly
does inflammation trigger pain?
Pain (like inflammation itself ) is
biologically and behaviorally necessary
(see "Understanding Inflammation's
Progression," Massage & Bodywork,
November/December 2018, page 98). Pain
protects against tissue damage by shaping
our behavior, while inflammation protects
against tissue damage by mobilizing
our immune system's physiological
safeguarding and repair functions. Both
of these kinds of protection—behavioral
and immunological—make sense when
danger or damage are actually present; but
both pain and inflammation can become
problematic when they chronically persist
after the threat is no longer around.
Also, keep in mind that pain and
nociception are not the same thing.
Nociception is a nerve signal indicating
potential mechanical, thermal, or chemical
threat to tissues; pain is the experience
the nervous system generates in response.
Many times, when your clients' pain
is prolonged, it can be because there is
continued nociceptive input (for example,
from ongoing mechanical or inflammatory
irritation). But pain can persist even
with little or no tissue damage; or, even
100 m a s s a g e & b o d y w o r k m a r c h / a p r i l 2 0 1 9
when there is
obvious damage or
degeneration, there
can be little or no
pain experience at all.
And while your
clients' pain may
not be as related
to physical tissue
damage as we might
have thought, there
turns out to be a
strong relationship
between pain and
expectations, fears,
context, memory,
and social influences.
These psychosocial
factors play a role
in inflammation,
as well as in pain.
For example, high
hostility scores have
been correlated
with increased inflammation, while openness
(hostility's flip-side) has been associated with
decreased inflammatory markers.
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But the
relationship between pain, inflammation, and
psychosocial factors is nuanced and complex:
while depressed people often have stronger
inflammatory responses, turning down
inflammation with immunosuppressive drugs
can also trigger depressive mood changes. So
even though pain, inflammation, and reactive
emotions are deeply interconnected, they don't
move in lockstep with one another. Instead,
they could be thought of as different modes
of physical, psychological, and behavioral
adaptation that we use in varying ways in the
face of perceived threat.
Musculoskeletal pain inflames both local
tissues and the brain. In a recent study
of sciatic pain (Loggia et al., 2015),
inflammation wasn't limited to the locally
painful tissues of the low back and leg. Glial
cells (inset), which play a key role in both
immunity and chronic pain, also respond
with inflammatory activation (orange) in
the corresponding regions of the brain's
sensory and motor cortexes. This has
implications for the use of both therapeutic
sensation (such as produced by touch) and
active client movement when working with
musculoskeletal inflammation. Motor cortex
image adapted from artwork by Giovanni
Rimasti, used by permission of Joseph E.
Muscolino (www.learnmuscles.com). Glial
cell micrograph adapted from H. Peluffo,
L. Acarin, M. Faiz, B. Castellano, and B.
Gonzalez, used under CCA 2.0G.
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